Abstract
Cadmium (Cd) has long been noted to induce neurodegenerative disorders. Therefore, this study aimed to assess the toxicological impact of Cd on rat brains and evaluate the possible ameliorative impact of omega-3 fatty acids as a protective agent of nervous system. Rats were divided into four groups: group I supplemented orally with saline; group II intoxicated with CdCl2 (5 mg/kg b.w. orally), and groups III and VI supplemented with omega-3 (100 mg/kg b.w. orally) simultaneously or before CdCl2 administration, respectively. Cd intoxication induced biochemical and histopathological disturbances in treated rats. Omega-3 fatty acid considerably improved the Cd-associated biochemical changes, reduced the elevation of lipid peroxidation, and normalized the Cd impact on the levels of superoxide dismutase, catalase, glutathione-S-transferases, 8-hydroxydeoxyguanosine, heatshock protein70, nuclear factor-κB, and interferon-γ as well as of neuronal enzymes such as acetylecholinesterase and monoamine oxidase within the brains of treated rats. Additionally, histological findings supported the results that Cd treatment-induced neurodegenerative changes and that polyunsaturated fatty acids act as antioxidants and neuroprotective agents against Cd toxicity. Co-treatment with omega-3 fatty acid was more beneficial than pretreatment. Thus, omega-3 fatty acid should be included in diet to prevent or suppress neurodegenerative disorders caused by continuous exposure to Cd.
Highlights
Cadmium (Cd) is a certainly occurring heavy metal possessing extreme dangers to human health
The influence of omega-3 fatty acids on the level of oxidative stress and antioxidant indices is demonstrated in Figs. 1 and 2
Ingestion of omega-3 fatty acids simultaneously with CdCl2 (GIII) or before CdCl2 (GIV) administration, successfully ameliorating the brain levels of oxidative stress index (MDA) and the enzymes of antioxidants in Cdintoxicated rats compared to intoxicated untreated ones
Summary
Cadmium (Cd) is a certainly occurring heavy metal possessing extreme dangers to human health. As oxidative stress is one of the necessary mechanisms of cadmium-induced damages, it will be expected that the administration of some antioxidants ought to be a crucial therapeutic approach (Renugadevi and Prabu 2010). Incorporation of DHA into cell membranes affects in lowering lipid peroxidation and oxidative pressure in neurons. The DHA reduces proinflammatory mediators and anti-inflammatory compounds in conjunction with materials that defend brain cells known as neuroprotectins (Bazan et al 2011). There are no reviews regarding the usage of omega-3 fat as a prophylactic agent against the toxicological effect of cadmium exposure in nervous system as it is far widely used as antioxidant and anti-inflammatory. The study might be extended to explore the effect of omega-3 fatty acid as a protecting agent with antioxidants and anti-inflammatory residences in a trial to minimize or suppress the cytotoxic impact of metallic Cd on nervous system. Histopathological studies of rat brain tissue might be examined to affirm the biochemical investigations
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